The proposed experiments examine the neuroendocrine control of drinking elicited by eating. First, the experiments evaluate the role of endogenous histamine as a component for drinking around mealtime in the rat by (1) evaluating pharmacologically the magnitude of a histaminergic component for drinking elicited by eating; (2) examining by vagotomy and pharmacological intervention) the role of vagal efferents and afferents and peripheral H1 and H2 receptors for histamine for (a) drinking in anticipation of a meal, and (b) drinking elicited by pregastric food-contingent stimulation during sham feeding in rats with open gastric fistulas; (3) examining pharmacologically the nature of antagonism of peripheral H1 and H2 receptors for drinking elicited by exogenous histamine; (4) evaluating pharmacologically the role of central nervous H1 and H2 receptors for drinking elicited by eating; and (5) evaluating pharmacologically a role for peripheral angiotensin II as a component for drinking elicited by eating in the rat. Second, these experiments consider the phenomenon of eating-elicited hyperdipsia in the spontaneously hypertensive rat (SHR) as a candidate mechanism for the development and/or maintenance of hypertension in SHR by (1) describing the development of food-contingent hyperdipsia; (2) examining pharmacologically for the mechanism(s) of food-contingent hyperdipsia; (3) describing the development of disordered drinking in response to stimuli which have been identified as components fo eating-elicited drinking--namely, systemic cellular dehydration, histamine and angiotensin II; (4) examining (by restricting access to water and by pharmacological intervention) the role of food-contingent hyperdipsia for the development of hypertension in SHR; and (5) examining (by restricting access to water and by pharmacological intervention) the role of food-contingent hyperdipsia for the maintenance of hypertension in adult SHR. The long-term objectives are (a) to direct future research for raddressing how endogenous histamine interacts with other multiple controls of drinking elicited by eating, and (b) to determine the relative extent to which disordered drinking around mealtime contributes to the development and/or maintenance of hypertension in an animal model for human essential hypertension.